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Transformation of normal cells by aberrant activation of YAP via cMyc with TEAD

Masazumi Nishimoto1,2, Kousuke Uranishi3, Masamitsu N Asaka3

  • 1Division of Developmental Biology, Research Center for Genomic Medicine, Saitama Medical University, 1397-1 Yamane Hidaka, Saitama, 350-1241, Japan. masamasa@saitama-med.ac.jp.

Scientific Reports
|July 31, 2019
PubMed

Insights

The Yes-associated protein (YAP) acts as a proto-oncogene, driving cell growth and tumorigenic transformation. Its aberrant activation, particularly with TEAD, promotes cancer by influencing cMYC, distinct from typical oncogenes.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Transcriptional Regulation

Background:

  • Yes-associated protein (YAP) is a transcriptional coactivator crucial for cell growth.
  • YAP is recognized as a proto-oncogene, but its precise role in cancer initiation is not fully understood.
  • Understanding YAP's oncogenic mechanisms is vital for cancer research.

Purpose of the Study:

  • To investigate the mechanism by which activated YAP induces tumorigenic transformation.
  • To elucidate the role of YAP in cooperation with transcription factors like TEAD.
  • To identify downstream effectors of YAP-mediated oncogenesis.

Main Methods:

  • Overexpression of YAP in NIH3T3 cells and mouse embryonic fibroblasts.
  • Analysis of YAP's interaction with transcription factors, specifically TEAD.
  • Assessment of downstream gene expression, including cMYC.

Main Results:

  • Overexpression of YAP alone was sufficient to induce tumorigenic transformation in NIH3T3 cells.
  • YAP functions in conjunction with the TEAD transcription factor to drive oncogenesis.
  • cMYC was identified as a critical downstream target of the YAP/TEAD complex.
  • Aberrant YAP activation also transformed non-immortalized mouse embryonic fibroblasts, bypassing senescence.

Conclusions:

  • YAP functions as a distinct type of proto-oncogene, driving tumorigenic transformation.
  • The YAP/TEAD complex, through cMYC, plays a pivotal role in YAP-induced oncogenesis.
  • YAP's oncogenic potential is linked to its ability to override normal cellular growth controls.

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